Stroke classification diagnosis management

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Here is a comprehensive review of stroke classification, diagnosis, and management.

Stroke: Classification, Diagnosis, and Management

Overview

Stroke is sudden neurological dysfunction from focal cerebral ischemia or hemorrhage. In the United States, about 600,000 first-ever ischemic strokes occur annually - one occurs every 40 seconds. It is the second leading cause of death worldwide, with an overall 30-day mortality of ~10%, 1-year mortality ~20%, and 5-year mortality ~40%.

Classification

Stroke classification: Hemorrhagic vs Ischemic

1. Ischemic Stroke (~80%)

Caused by absence of blood - insufficient oxygen and nutrient delivery. Three main mechanisms:
SubtypeProportionMechanism
Thrombotic (large-vessel)~1/3Atherosclerotic plaque ulceration + clot at vessel bifurcations (ICA most common)
Lacunar (small-vessel)~1/4Lipohyalinosis of penetrating arteries; basal ganglia, thalamus, pons, internal capsule; 80-90% have HTN
Cardioembolic~1/4Atrial fibrillation is most common (5x risk); also mural thrombus, valvular disease
Cryptogenic>1/3No clear cause identified
Special causes in young patients (<45 years, ~3-4% of strokes):
  • Carotid/vertebral dissection (leading determined cause in the young - may follow minor trauma, sneezing, yoga, spinal manipulation)
  • Antiphospholipid syndrome, protein C/S deficiency
  • Oral contraceptives, pregnancy
  • Sickle cell anemia, polycythemia
  • Fibromuscular dysplasia
  • Cocaine/amphetamine vasospasm
  • Varicella or fungal vasculopathy

Transient Ischemic Attack (TIA)

Transient neurologic dysfunction from focal ischemia without acute infarction. Risk of stroke after TIA: up to 10% at 2 days and 15% at 90 days - a medical emergency.

2. Hemorrhagic Stroke (~20%)

Caused by presence of blood - mechanical compression of brain tissue plus local toxicity from blood breakdown products. Higher acute morbidity/mortality (30-day mortality ~50%, vs ~10% for ischemic).
Two anatomic subtypes:
A. Intracerebral Hemorrhage (ICH)
  • Risk factors: hypertension (most common), older age, Black/Asian race, high alcohol use, low LDL/triglycerides
  • Causes: hypertension, cerebral amyloid angiopathy (CAA in elderly), AVM, coagulopathy, anticoagulant use, tumor, cocaine
  • CT appearance: round/oval hyperdense lesion (40-60 HU early, 80-100 HU over days)
Noncontrast CT showing intracerebral hemorrhage - hyperdense (bright) area in right temporal lobe
Noncontrast CT: Hyperdense lesion (arrow) in right temporal lobe = intracerebral hemorrhage - Frameworks for Internal Medicine
B. Subarachnoid Hemorrhage (SAH)
  • Bleeding between arachnoid and pia mater
  • Classic: thunderclap headache ("worst headache of my life"), ruptured aneurysm
  • CT may miss; LP shows xanthochromia if CT negative

Stroke Mimics (Differential Diagnosis)

Must exclude before treating:
  • Hypoglycemia (most important - can mimic stroke for days)
  • Todd's paralysis (postictal focal weakness)
  • Subdural/epidural hematoma
  • Brain tumor or abscess
  • Complex migraine with aura
  • Wernicke encephalopathy (ophthalmoplegia + ataxia + confusion mimics cerebellar stroke)
  • Bell's palsy, vestibular neuronitis, Ménière disease
  • Giant cell arteritis

Diagnosis

Immediate Evaluation (NINDS Target Times)

StepTarget Time
Door to physician10 min
Door to CT completion25 min
Door to CT interpretation45 min
Door to treatment60 min
Neurology access15 min
Neurosurgery access2 hours

Neuroimaging

Non-contrast CT head (first-line):
  • Immediately distinguishes ischemic from hemorrhagic stroke
  • Highly sensitive for parenchymal hemorrhage >1 cm and SAH
  • Early ischemic changes (within 3 hours): hyperdense artery sign, sulcal effacement, loss of insular ribbon, gray-white interface loss, acute hypodensity (seen in up to 67% within 3 hours)
  • Gross infarct signs typically not visible for 6-12 hours
CT Angiography (CTA):
  • Run concurrently with CT head
  • Identifies large vessel occlusion (LVO) for thrombectomy triage
  • Also detects dissection, stenosis
CT Perfusion (CTP):
  • Identifies salvageable penumbra in extended time windows (6-24 hours)
  • Generally not needed in first 6 hours
MRI:
  • Much higher sensitivity for ischemic stroke than CT, especially posterior fossa and within first hours
  • DWI-FLAIR mismatch: DWI-positive + FLAIR-negative = stroke likely within ~4.5 hours (useful for "wake-up" strokes)
  • Standard imaging for thrombectomy in 6-24 hour window (DAWN/DEFUSE-3 protocols)

Other Workup

  • ECG - identify AF and acute MI
  • Blood glucose - immediately (hypo/hyperglycemia mimics stroke)
  • CBC, coagulation studies, BMP, troponin
  • Echocardiography - cardioembolic source
  • Carotid duplex / CTA neck - stenosis, dissection
  • Cardiac monitoring (48-72h or longer) - paroxysmal AF detection

Management

A. General Supportive Care (All Stroke Types)

  • Airway/Breathing/Circulation - supplemental O2 only if SpO2 <94%
  • IV access - avoid overhydration (cerebral edema risk); use isotonic saline; avoid dextrose solutions in normoglycemic patients
  • Temperature - treat fever (>38°C) aggressively; even mild hyperthermia worsens neurologic injury
  • Blood glucose - target 140-180 mg/dL; treat hypoglycemia (<60 mg/dL) with IV dextrose
  • Swallowing assessment - NPO until evaluated (aspiration risk)
  • Document exact time of last known well - determines eligibility for reperfusion

B. Ischemic Stroke Management

Blood Pressure

  • Without thrombolysis: withhold antihypertensives unless SBP >220 mmHg, DBP >120 mmHg, or MAP >130 mmHg (permissive hypertension preserves penumbral perfusion)
  • Before thrombolysis: lower to <185/110 mmHg before starting tPA
  • After thrombolysis: maintain <180/105 mmHg for 24 hours; monitor BP every 15 min during infusion, then every 30 min for 6h, then hourly for 16h
Agents for pre-thrombolysis BP control:
  • Labetalol 10-20 mg IV over 1-2 min (may repeat once)
  • Nicardipine infusion 5 mg/h, titrate by 2.5 mg/h every 5-15 min (max 15 mg/h)
  • Clevidipine 1-2 mg/h IV, double dose every 2-5 min (max 21 mg/h)

Reperfusion Therapy

1. IV Thrombolysis (tPA)
Alteplase
  • Dose: 0.9 mg/kg IV (max 90 mg); 10% as bolus over 1 min, remainder over 60 min
  • Time window: within 3 hours (FDA-approved); up to 4.5 hours for eligible patients
  • Contraindications include: recent surgery, active bleeding, prior ICH, BP consistently >185/110 mmHg (untreated), INR >1.7, heparin use within 48h with elevated aPTT, glucose <50 or >400 mg/dL
Tenecteplase (TNK-tPA)
  • Single IV bolus, simpler administration; approved as alternative
  • Dose: 0.25 mg/kg IV (max 25 mg)
Extended window (3-4.5 hours) - additional exclusions apply: age >80, NIHSS >25, prior stroke + DM, oral anticoagulant use
Mild nondisabling stroke (NIHSS 0-5): IV alteplase NOT recommended (PRISMS trial: no benefit over aspirin, 78% vs 82% favorable outcome)
Mild disabling stroke: IV alteplase IS recommended within 3-4.5 hours
2. Mechanical Thrombectomy (Endovascular)
  • For large vessel occlusion (LVO) confirmed on CTA (ICA, M1/M2 MCA, basilar artery)
  • Time window: 0-6 hours (standard); 6-24 hours in selected patients with favorable penumbra imaging (DAWN/DEFUSE-3 criteria: target mismatch on CTP or DWI/PWI-MRI)
  • Maintain BP ≤185/110 mmHg pre-procedure (if no prior IV tPA)
  • Give IV tPA first if eligible; do NOT delay tPA to wait for thrombectomy

Antiplatelet Therapy

  • Aspirin 325 mg within 24-48 hours of ischemic stroke (not within 24h of tPA)
  • For minor stroke / high-risk TIA: dual antiplatelet (aspirin + clopidogrel) for 21 days (POINT/CHANCE trial evidence)
  • Anticoagulation for cardioembolic stroke (AF): start after 4-14 days depending on stroke size; DOAC preferred over warfarin

C. Hemorrhagic Stroke Management

Intracerebral Hemorrhage (ICH)

  • Reverse coagulopathy immediately: elevated INR - give vitamin K + 4-factor PCC (or FFP); dabigatran - idarucizumab; Xa inhibitors - andexanet alfa
  • Blood pressure: if SBP 150-220 mmHg, acute lowering to target SBP 140 mmHg is safe and reasonable; reduces hematoma expansion
  • Seizure prophylaxis: treat clinical seizures with antiepileptics; prophylactic treatment controversial
  • Intracranial pressure management if elevated: HOB elevation 30°, hypertonic saline, osmotic therapy (mannitol), intubation/sedation, hemicraniectomy in refractory cases
  • Glucose management: avoid hyper- and hypoglycemia
  • Surgical evacuation: consider for cerebellar hemorrhage >3 cm, or accessible lobar clot with deterioration; deep basal ganglia hemorrhage generally not operated (no mortality benefit)
ICH Score (predicts 30-day mortality):
FeaturePoints
GCS 3-42
GCS 5-121
GCS 13-150
ICH volume >30 mL1
Intraventricular hemorrhage1
Infratentorial origin1
Age >801
30-day mortality: score 0 = ~0%; score 1 = ~13%; score 2 = ~26%; score 4-5 = ~97%

Subarachnoid Hemorrhage (SAH)

  • Neurosurgical/neurovascular emergency
  • Secure aneurysm (coiling or clipping) early
  • Nimodipine 60 mg q4h for 21 days (reduces vasospasm-related deficit)
  • Monitor for hydrocephalus (external ventricular drain)
  • Triple-H therapy (hypertension, hypervolemia, hemodilution) for delayed cerebral ischemia (vasospasm)

Stroke Risk Factors and Secondary Prevention

Modifiable risk factors:
  • Hypertension (strongest risk factor - present in most stroke patients; SBP ≥140 or DBP ≥90 mmHg)
  • Atrial fibrillation (~5x risk)
  • Diabetes mellitus
  • Dyslipidemia
  • Smoking
  • Physical inactivity
Secondary prevention (ischemic stroke):
  • Antiplatelet therapy (aspirin, clopidogrel, or aspirin + dipyridamole)
  • Anticoagulation for AF (DOAC preferred)
  • Statin therapy (high-intensity)
  • Carotid endarterectomy or stenting if symptomatic stenosis >50% (CEA preferred for >70%)
  • BP control (target <130/80 mmHg)
  • Lifestyle modification

Prognosis

TimeframeMortality
30-day (overall)~10%
30-day (ICH)~50%
1-year~20%
5-year~40%
Worse prognosis with: older age, comorbid CAD or DM, larger infarct size, posterior circulation involvement.

Sources: ROSEN's Emergency Medicine: Concepts and Clinical Practice, 9e; Frameworks for Internal Medicine; Bradley and Daroff's Neurology in Clinical Practice

Clinical features

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I now have thorough textbook data on all stroke territory syndromes. Here is the comprehensive clinical features answer.

Clinical Features of Stroke

Stroke features are best understood by the vascular territory affected. The key principle: anterior circulation (ICA, ACA, MCA) governs hemispheric functions (motor, sensory, language, cognition), while posterior circulation (vertebral, basilar, PCA, cerebellar arteries) governs brainstem reflexes, cranial nerve function, coordination, and vision.

General Presenting Features

Any of the following sudden-onset symptoms should raise immediate suspicion:
  • Unilateral face/arm/leg weakness or numbness
  • Speech difficulty (aphasia or dysarthria)
  • Visual disturbance (monocular loss, hemianopia, diplopia)
  • Severe headache (especially hemorrhagic stroke - "worst ever")
  • Vertigo, ataxia, imbalance
  • Altered consciousness or confusion
Headache occurs in 25-30% of ischemic strokes (more common in posterior than anterior circulation). Seizures occur in 3-10%, usually after onset, occasionally as the presenting feature.

Anterior Circulation Syndromes

Internal Carotid Artery (ICA)

  • Ipsilateral amaurosis fugax - transient monocular blindness from emboli to the ophthalmic artery (this distinguishes ICA from pure MCA syndrome)
  • Contralateral hemiplegia, hemisensory loss
  • Homonymous hemianopia
  • Aphasia if dominant hemisphere

Middle Cerebral Artery (MCA) - Most Common Stroke Territory

MCA DivisionClinical Features
Stem (complete MCA)Contralateral hemiplegia, hemianesthesia, homonymous hemianopia; conjugate ipsilateral eye deviation; global aphasia (dominant) or hemineglect (non-dominant)
Upper divisionFace and arm > leg weakness; Broca's aphasia (dominant) - non-fluent speech, poor repetition, intact comprehension; impaired prosody (non-dominant)
Lower divisionWernicke's aphasia (dominant) - fluent but meaningless speech, poor comprehension; behavioral disturbances (non-dominant); homonymous hemianopia
Lenticulostriate branchesPure motor hemiparesis from internal capsule lacune (subcortical - no aphasia, no sensory loss)
Additional dominant-hemisphere MCA features:
  • Alexia with agraphia (angular gyrus)
  • Gerstmann syndrome (left angular/parietal gyrus): finger agnosia + acalculia + right-left disorientation + agraphia
  • Conduction aphasia, transcortical aphasia (depending on extent)
  • Anosognosia (denial of hemiparesis, more common with right hemisphere lesions)
Non-dominant hemisphere features:
  • Hemi-inattention, tactile and visual extinction
  • Anosognosia, anosodiaphoria
  • Apraxia, impaired prosody
  • Acute agitated delirium (rarely)

Anterior Cerebral Artery (ACA) - <3% of infarcts

  • Contralateral leg > arm weakness (the leg is represented medially, which is ACA territory)
  • Discriminative and proprioceptive sensory loss (lower extremity)
  • Abulia (reduced motivation, flat affect)
  • Akinetic mutism with bilateral mesiofrontal damage
  • Transcortical motor aphasia (dominant hemisphere)
  • Left arm apraxia (anterior corpus callosum disconnection)
  • Sphincter incontinence
  • Paratonia (gegenhalten)
CT showing right ACA territory infarction causing left-sided weakness and abulia
CT showing right ACA territory infarction - the hypodense (dark) area in the right frontal/medial region - Bradley and Daroff's Neurology

Anterior Choroidal Artery

Classic triad:
  1. Hemiparesis (posterior limb of internal capsule)
  2. Hemisensory loss (posterolateral thalamus or thalamocortical fibers)
  3. Hemianopia (lateral geniculate body or geniculo-calcarine tract) - with characteristic sparing of the horizontal meridian

Lacunar Syndromes (Small-Vessel / Deep Perforator Occlusion)

Lacunes are 0.5-15 mm infarcts in deep brain structures - basal ganglia, thalamus, internal capsule, pons, corona radiata. At least 20 syndromes described; the 5 classic ones are:
SyndromeKey FeaturesCommon Location
Pure Motor HemiparesisContralateral face, arm, and leg weakness + dysarthria; NO sensory/visual/cortical signsPosterior limb internal capsule, basis pontis, corona radiata
Pure Sensory StrokeParesthesia, numbness, unilateral hemisensory loss (all modalities)VPL/VPM thalamus
Sensorimotor StrokeMotor + sensory deficit combinedPosterior internal capsule + thalamus
Ataxic HemiparesisHemiparesis + ipsilateral limb ataxia (cerebellar signs on same side as weakness)Posterior internal capsule or basis pontis
Dysarthria - Clumsy Hand SyndromeSupranuclear facial weakness + dysarthria + dysphagia + loss of fine hand motor control + Babinski signDeep basis pontis
Lacunar features distinguishing them from cortical strokes: no aphasia, no apraxia, no agnosia, no visual field defect, no hemineglect. Multiple lacunes can cause vascular dementia.

Posterior Circulation Syndromes

Posterior Cerebral Artery (PCA)

FeatureMechanism
Contralateral homonymous hemianopia (often with macular sparing)Striate cortex / optic radiations infarction
Superior quadrantanopiaStriate cortex inferior to calcarine / inferior optic radiations
Inferior quadrantanopiaSuperior to calcarine / superior optic radiations
Alexia without agraphiaLeft occipital lobe + splenium of corpus callosum (can write, cannot read)
Visual hallucinations (formed or unformed)Occipital cortex
Prosopagnosia, color agnosiaOccipital/temporal
Dejerine-Roussy syndromeContralateral sensory loss + thalamic pain (severe dysesthesias) + choreoathetosis + transient hemiparesis
Anton syndromeBilateral occipital - cortical blindness with denial/unawareness of blindness
Balint syndromeBilateral parieto-occipital - optic ataxia + optic apraxia + simultanagnosia
Global amnesiaLeft medial temporal or bilateral mesiotemporal involvement

Thalamic Infarction

RegionFeatures
Posterolateral (thalamogeniculate a.)Pure sensory stroke, sensorimotor stroke, Dejerine-Roussy syndrome
Anterior (polar/tuberothalamic a.)Memory impairment, emotional disturbances, dysphasia (left) or neglect (right)
ParamedianClassic triad: decreased consciousness + memory loss + vertical gaze palsy
Dorsal (posterior choroidal a.)Homonymous quadrantanopia or horizontal sectoranopsia
Bilateral (artery of Percheron)Bilateral thalamic infarction: coma, amnesia, vertical gaze palsy

Cerebellar Syndromes

ArterySyndromeFeatures
PICA (medial branch)VestibulocerebellarProminent vertigo, ataxia, nystagmus
PICA (lateral branch)-Vertigo, gait ataxia, limb dysmetria, nausea/vomiting, conjugate gaze palsies, dysarthria
PICA / Vertebral arteryWallenberg (lateral medullary) syndromeIpsilateral: Horner syndrome, facial pain/temperature loss, palate/pharynx/cord weakness, cerebellar ataxia. Contralateral: hemibody pain/temperature loss
AICALateral inferior pontineIpsilateral: facial palsy, facial sensory loss, corneal hyesthesia, deafness, Horner, ataxia. Contralateral: hemibody pain/temperature loss
SCADorsal cerebellarIpsilateral: Horner, nystagmus, ataxia, intention tremor. Contralateral: hearing loss, hemibody hypalgesia. Vertigo less prominent than PICA

Brainstem Syndromes

Midbrain

SyndromeFeatures
WeberIpsilateral CN III palsy (dilated pupil, ptosis, "down and out" eye) + contralateral hemiplegia
BenediktIpsilateral CN III palsy + contralateral involuntary movements (tremor, hemiballismus, hemichorea) - red nucleus involvement
ClaudeIpsilateral CN III palsy + contralateral cerebellar signs (more dorsal than Benedikt)
ParinaudSupranuclear upward gaze paralysis + convergence-retraction nystagmus + pupillary light-near dissociation + lid retraction
Top of basilarSomnolence, peduncular hallucinosis, memory disturbances, ocular motor abnormalities, hemianopia or cortical blindness

Pons

SyndromeFeatures
Locked-in syndrome (bilateral ventral pons)Quadriplegia + aphonia + loss of horizontal gaze; preserved consciousness; vertical eye movement and blinking intact
Lateral inferior pontine (AICA)Ipsilateral: facial palsy, facial sensory loss, conjugate gaze palsy, deafness, tinnitus, ataxia. Contralateral: hemibody pain/temperature loss
Medial inferior pontine (paramedian basilar branch)Ipsilateral: conjugate gaze palsy, abducens palsy, nystagmus, ataxia. Contralateral: hemibody tactile/proprioceptive loss + hemiparesis

Medulla

SyndromeFeatures
Lateral medullary (Wallenberg)Vertebral artery >> PICA. Ipsilateral: Horner, facial pain/temp loss, palatal/pharyngeal/laryngeal weakness, ataxia. Contralateral: hemibody pain/temp loss
Medial medullary (Dejerine)Ipsilateral: lower motor neuron tongue paralysis (tongue deviates to lesion side). Contralateral: hemiparesis (face spared) + loss of tactile/vibratory/position sense

Watershed (Border Zone) Infarctions

Occur during hypoperfusion (cardiac arrest, shock, severe bilateral carotid stenosis):
TerritoryClinical Picture
ACA/MCA bilateral"Man in a barrel" - bilateral proximal arm weakness with preserved leg function; impaired saccadic eye movements
MCA/PCA bilateralBilateral parieto-occipital - cortical blindness, dyslexia, dyscalculia, memory deficits
ACA/MCA/PCABilateral lower visual field defects, optic ataxia, cortical blindness

Hemorrhagic Stroke: Clinical Clues

Features favoring hemorrhagic over ischemic stroke:
  • Sudden, severe headache at onset ("thunderclap")
  • Rapid progression to coma or obtundation
  • Vomiting at onset
  • Very high blood pressure at presentation
  • Stiff neck (suggests SAH)
  • Onset during exertion
Note: imaging is required to differentiate - clinical features alone cannot reliably distinguish hemorrhagic from ischemic stroke.

NIHSS Assessment

The National Institutes of Health Stroke Scale (NIHSS) quantifies stroke severity at bedside across 11 domains: consciousness, gaze, visual fields, facial palsy, arm/leg motor, limb ataxia, sensory, language, dysarthria, and extinction/inattention.
  • Mild: NIHSS 1-4
  • Moderate: NIHSS 5-15
  • Severe: NIHSS 16-20
  • Very severe: NIHSS >20

Sources: Bradley and Daroff's Neurology in Clinical Practice; Neuroanatomy through Clinical Cases, 3rd Edition; ROSEN's Emergency Medicine, 9e
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